Connective tissue growth factor: a novel player in tissue reorganization after brain injury?

Hertel, Moritz; Tretter, Y; Alzheimer, Christian; Werner, Sabine

doi:10.1046/j.1460-9568.2000.00930.x

Cited by 57 publications

(53 citation statements)

References 25 publications

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“…CTGF is found to occur at elevated levels in a variety of fibrotic pathologies, including the fibrous stroma of mammary tumors (Frazier and Grotendorst, 1997), chronic pancreatitis (di Mola et al, 1999), cataract formation (Wunderlich et al, 2000), nephropathy (Ito et al, 1998;Wang et al, 2001), systemic sclerosis (Sato et al, 2000), pulmonary fibrosis (Lasky et al, 1998;Sato et al, 2000), inflammatory bowel disease (Dammeier et al, 1998), bladder fibrosis due to outlet obstruction (Chaqour et al, 2002), brain fibrosis following injury (Hertel et al, 2000), atherosclerosis (Fan et al, 2000), and fibrotic skin disorders (Igarashi et al, 1996). CTGF alone does not promote fibrosis.…”

Section: Ctgf and Fibrosismentioning

confidence: 99%

Connective Tissue Metabolism and Gingival Overgrowth

Trackman

Kantarcı

2004

Critical Reviews in Oral Biology & Medicine

135

152

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Gingival overgrowth occurs mainly as a result of certain anti-seizure, immunosuppressive, or antihypertensive drug therapies. Excess gingival tissues impede oral function and are disfiguring. Effective oral hygiene is compromised in the presence of gingival overgrowth, and it is now recognized that this may have negative implications for the systemic health of affected patients. Recent studies indicate that cytokine balances are abnormal in drug-induced forms of gingival overgrowth. Data supporting molecular and cellular characteristics that distinguish different forms of gingival overgrowth are summarized, and aspects of gingival fibroblast extracellular matrix metabolism that are unique to gingival tissues and cells are reviewed. Abnormal cytokine balances derived principally from lymphocytes and macrophages, and unique aspects of gingival extracellular matrix metabolism, are elements of a working model presented to facilitate our gaining a better understanding of mechanisms and of the tissue specificity of gingival overgrowth.

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Section: Ctgf and Fibrosismentioning

confidence: 99%

Connective Tissue Metabolism and Gingival Overgrowth

Trackman

Kantarcı

2004

Critical Reviews in Oral Biology & Medicine

135

152

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“…Others have also reported significant induction of neuronal damage in the CA3 and CA1 subregions of the hippocampus in C57BL/6 mice in response to kainate-induced seizures. 85,86 Thus, it is not clear why Schauwecker and Steward failed to It is well recognized that there is a substantial genetic variability among the 129 substrains with documented phenotypic differences. 88 The variable contribution from the C57BL/6 background in the two p53 knock-out mouse strains in combination with other variations in the genetic make-up of the mice used in these experiments make it difficult to draw firm conclusions regarding the role of the purported protective genes in kainic acid-induced neuronal damage seen with one p53 knock-out mouse strain but not the other.…”

Section: The Relationship Between P53 Expression and Neuronal Cell Deathmentioning

confidence: 99%

The role of p53 in neuronal cell death

2000

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The p53 tumor suppressor gene is a sequence-specific transcription factor that activates the expression of genes engaged in promoting growth arrest or cell death in response to genotoxic stress. A possible role for p53-related modulation of neuronal viability has been suggested by the finding that p53 expression is elevated in damaged neurons in acute models of injury such as ischemia and epilepsy and in brain tissue samples derived from patients with chronic neurodegenerative diseases. Moreover, the absence of p53 has been shown to protect neurons from a wide variety of acute toxic insults. Signal transduction pathways associated with p53-induced cell death are being unraveled and suggest that intervention may prove fruitful in maintaining neuronal viability and restoring function following cytopathic insults.

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“…Throughout the central nervous system, CTGF protein is found in astrocytes, as well as in neuronal cells of the cortex, where it supposedly mediates TGF-␤-related functions in cell growth, development, and tissue remodeling following injury (67,68). NOVR was expressed in cortical layers II/III, V, and VI, in the CA1-CA3 hippocampus region and the amygdala, which are major parts of the basal forebrain cholinergic system, but its expression did not change in response to mAChR stimulation.…”

Section: Fig 5 Muscarinic Receptor Subtypes Differently Inducementioning

confidence: 99%

Muscarinic Acetylcholine Receptors Induce the Expression of the Immediate Early Growth Regulatory Gene CYR61

Albrecht¹,

Kammer²,

Mayhaus³

et al. 2000

Journal of Biological Chemistry

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In brain, muscarinic acetylcholine receptors (mAChRs) modulate neuronal functions including long term potentiation and synaptic plasticity in neuronal circuits that are involved in learning and memory formation. To identify mAChR-inducible genes, we used a differential display approach and found that mAChRs rapidly induced transcription of the immediate early gene CYR61 in HEK 293 cells with a maximum expression after 1 h of receptor stimulation. CYR61 is a member of the emerging CCN gene family that includes CYR61/CEF10, CTGF/FISP-12, and NOV; these encode secretory growth regulatory proteins with distinct functions in cell proliferation, migration, adhesion, and survival. We found that CYR61, CTGF, and NOV were expressed throughout the human central nervous system. Stimulation of mAChRs induced CYR61 expression in primary neurons and rat brain where CYR61 mRNA was detected in cortical layers V and VI and in thalamic nuclei. In contrast, CTGF and NOV expression was not altered by mAChRs neither in neuronal tissue culture nor rat brain. Receptor subtype analyses demonstrated that m1 and m3 mAChR subtypes strongly induced CYR61 expression, whereas m2 and m4 mAChRs had only subtle effects. Increased CYR61 expression was coupled to mAChRs by both protein kinase C and elevations of intracellular Ca 2؉ . Our results establish that CYR61 expression in mammalian brain is under the control of cholinergic neurotransmission; it may thus be involved in cholinergic regulation of synaptic plasticity.

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Connective tissue growth factor: a novel player in tissue reorganization after brain injury?

Cited by 57 publications

References 25 publications

Connective Tissue Metabolism and Gingival Overgrowth

Connective Tissue Metabolism and Gingival Overgrowth

The role of p53 in neuronal cell death

Muscarinic Acetylcholine Receptors Induce the Expression of the Immediate Early Growth Regulatory Gene CYR61

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